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Hypoxia-induced regulation of the very low density lipoprotein receptor

Artikel i vetenskaplig tidskrift
Författare Jeanna Perman Sundelin
Ulf Lidberg
Ali Moussavi Nik
Peter Carlsson
Jan Borén
Publicerad i Biochemical and Biophysical Research Communications
Volym 437
Nummer/häfte 2
Sidor 274-279
ISSN 0006-291X
Publiceringsår 2013
Publicerad vid Wallenberglaboratoriet
Institutionen för kemi och molekylärbiologi
Institutionen för medicin, avdelningen för molekylär och klinisk medicin
Sidor 274-279
Språk en
Länkar dx.doi.org/10.1016/j.bbrc.2013.06.0...
Ämnesord Very low density lipoprotein receptor, Hypoxia inducible factor 1 alpha, Hypoxia responsive element, TRANSCRIPTIONAL REGULATION, ADIPOCYTE DIFFERENTIATION, BINDING PROTEIN, MESSENGER-RNA, EXPRESSION, GENE, ACTIVATION, PROMOTER, ELEMENTS, ENHANCER, KAHASHI S, 1992, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
Ämneskategorier Klinisk medicin

Sammanfattning

The very low density lipoprotein receptor (VLDLr) is highly upregulated during hypoxia in mouse cardiomyocytes and in human and mouse ischemic hearts causing a detrimental lipid accumulation. To know how the gene is regulated is important for future studies. In this study, we have thoroughly mapped the 5 '-flanking region of the mouse VLDLr promoter and show that the hypoxia-mediated increase in VLDLr expression is dependent on Hif-1 alpha, binding to a hypoxia responsive element (HRE) located at -162 to-158 bp 5 ' of translation start. We show that classical HRE sites and the previously described PPAR gamma and Sp1 binding are not involved in the hypoxia-induced regulation of the VLDLr promoter. Using a chromatin immunoprecipitation (ChIP) assay, we show that Hif-1 alpha t specifically binds and activates the mouse VLDLr promoter at the previously described non-classical HRE in HL-1 cells. We also show that the same HRE is present and active in response to hypoxia in human cardiomyocytes, however at a different location (-812 bp from translation start). These results conclude that in the hypoxic hearts of mice and men, the VLDLr gene is regulated by a direct binding of Hif-1 alpha to the VLDLr promoter. (C) 2013 Elsevier Inc. All rights reserved.

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